Abstract
Epidermal growth factor receptor (EGFR) inhibitors are widely used to treat various types of cancers such as non-small cell lung cancer, head and neck cancer, breast cancer, pancreatic cancer. Adverse reactions such as skin toxicity, interstitial lung disease, hepatotoxicity, ocular toxicity, hypomagnesemia, stomatitis, and diarrhea may occur during treatment. Because the EGFR signaling pathway is important for maintaining normal physiological skin function. Adverse skin reactions occurred in up to 90% of cancer patients treated with EGFR inhibitors, including common skin toxicities (such as papulopustular exanthemas, paronychia, hair changes) and rare fatal skin toxicities (e.g., Stevens–Johnson syndrome, toxic epidermal necrolysis, acute generalized exanthematous pustulosis). This has led to the dose reduction or discontinuation of EGFR inhibitors in the treatment of cancer. Recently, progress has been made about research on the skin toxicity of EGFR inhibitors. Here, we summarize the mechanism of skin toxicity caused by EGFR inhibitors, measures to prevent severe fatal skin toxicity, and provide reference for medical staff how to give care and treatment after adverse skin reactions.
Highlights
The epidermal growth factor receptor (EGFR, named HER1) is a 170 kDa transmembrane glycoprotein receptor that is coded by the c-erbB1 proto-oncogene located on the human 7q22 chromosome [1]
Del19, exon 19 deletion; L858R, exon 21 mutations; T790M, mutation of the 790th amino acid threonine of Epidermal growth factor receptor (EGFR) to methionine; C797S, cysteine is replaced by serine at position 797; EGFR, epidermal growth factor receptor; TKIs, tyrosine kinase inhibitors; NSCLC, non-small cell lung cancer; AGEP, acute generalized exanthematous pustulosis; TEN, toxic epidermal necrolysis; NME, necrolytic migratory erythema; SJS, Stevens-Johnson syndrome; HER, human epidermal growth factor receptor; DIHS, drug-induced hypersensitivity syndrome; ALK, anaplastic lymphoma kinase; IGF-1R, insulin-like growth factor-1 receptor; FLT-3, fms-like tyrosine kinase 3; Ig, immunoglobulin; mCRC, metastatic colorectal cancer
Up to 90% of cancer patients treated with EGFR inhibitors have skin adverse reactions
Summary
The epidermal growth factor receptor (EGFR, named HER1) is a 170 kDa transmembrane glycoprotein receptor that is coded by the c-erbB1 proto-oncogene located on the human 7q22 chromosome [1]. EGFR is highly expressed in lung cancer [4], breast cancer, human glioblastoma [5], gastric carcinoma [3], rectal cancer, and head and neck cancer [6] compared to healthy tissues. The EGFR signaling pathway is involved in normal biological processes of cells, and the destruction of the dynamic balance will lead to pathological changes in healthy tissues. Overexpression of EGFR promotes cell proliferation, adhesion, metastasis, and angiogenesis and inhibits apoptosis, all of which can induce tumorigenesis [7].
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